• Professor and Director of the Glaucoma Service (1991 to present) as well as Chairman of the Department of Ophthalmology and Visual Sciences (2000 to present) at the University of Nebraska Medical Center in Omaha
• First person to document the concept that prostaglandins might reduce IOP and therefore be useful in glaucoma therapy, 1975
• Principal investigator for a multiyear NIH grant (R01EY007865) to study the prostaglandin-induced reduction of IOP in animals and humans, 1988 to 1996
• Principal investigator for the pivotal FDA phase 3 clinical trial (1993 to 1995) involving 17 centers and 268 patients in the US that demonstrated the greater efficacy of latanoprost than timolol6 and led to the drug's approval for glaucoma therapy in 1996
• Inventor of a novel glaucoma drainage device based on his idea from 1983 that was initially patented in 1994

1. How would you describe your interactions with Laszlo Bito, PhD, in the proof of concept for the prostaglandin-induced lowering of IOP?
I closely collaborated with Dr. Bito from 1976, when I was a first-year medical student working in his laboratory, until 2001, when he retired from his scientific career. He is the person who is most responsible for developing prostaglandin analogs to the point of clinical usage. Without question, our patients would not be benefiting from latanoprost today if it were not for his innumerable, invaluable contributions. He clearly was the overall leader of this project.

Based on unrelated studies that I had conducted as an undergraduate student at Yale University in New Haven, Connecticut, I proposed that prostaglandins might reduce IOP and be useful in glaucoma therapy. Although my senior research adviser at Yale did not feel that my idea had merit, his opinion did not discourage me from pursuing my strong feelings and thoughts. Familiar with Dr. Bito's previous publications on the active transport of prostaglandins from ocular tissues,1,2 I sought his help after I left Yale to begin medical school at the Columbia College of Physicians and Surgeons in New York. He was intrigued by my idea. In 1976, we demonstrated the ocular hypotensive effect of topically applied prostaglandins in rabbits3 and later in monkeys4 for the first time. Our work also included a glaucomatous monkey eye, which demonstrated a reduction in IOP of greater than 35 mm Hg in response to a high dose of a prostaglandin. We continued to collaborate on many projects thereafter, including one of the first clinical trials evaluating the effects of the topical application of prostaglandins in patients with ocular hypertension or glaucoma.5

I feel that few people, if anyone, could have taken this project to fruition as successfully as Dr. Bito did. Because of his seminal contributions, millions of patients throughout the world are benefiting from the most successful class of medications in ophthalmology.

Dr. Bito was generous in his support of me on a personal level and in my academic career. Without him, I could not possibly have accomplished all that I have or attained the academic positions that I hold. I will value his tremendous influence on my personal life as a close friend, mentor, collaborator, colleague, and confidant forever.

2. How did your training under Steven Podos, MD, influence you as an ophthalmologist?
I had the privilege of completing my Heed Fellowship (1983 to 1984) in glaucoma under the direction of Dr. Podos at the Mt. Sinai Medical Center in New York. I was attracted to the opportunity by his tremendous accomplishments as an academician and leader as well as by his previous work in the field of prostaglandins. It was a special year from an educational, research, and clinical perspective. Based on my earlier studies with Dr. Bito and during my ophthalmology residency, I wanted to pursue my work with prostaglandins. During my glaucoma fellowship, Dr. Podos and I scientifically demonstrated for the first time that a reduction of IOP could be maintained by the repeated dosing of topically applied prostaglandins in monkeys. I remained on the full-time faculty at Mt. Sinai with him for 7 years after completing my fellowship.

Without question, my interactions with Dr. Podos were vital in advancing my academic and clinical career in glaucoma. His incomparable intellect and great wisdom helped me in so many ways. In addition to providing the encouragement and proper milieu for productive animal and clinical research, Dr. Podos gave me a foundation of knowledge that has enabled me to provide the highest quality of clinical and surgical care to my glaucoma patients. I cannot begin to describe the wealth of information that I acquired under his tutelage. As a special mentor and friend, Dr. Podos deserves particular thanks for teaching me about glaucoma, research, and life.

3. What impact did the late Michael Yablonski, MD, PhD, have on your career path?
Dr. Yablonski was an outstanding recruiter who convinced me to leave my academic position in New York in order to join him as Vice Chair and Director of the Glaucoma Service in the Department of Ophthalmology at the University of Nebraska Medical Center. One year earlier, he, too, had left his academic position in New York to assume the position of chair. As its only two clinical faculty members, we had plans to build the department in a very livable and family-oriented part of the country.

Dr. Yablonski was an original, innovative thinker who made several influential contributions to the field of glaucoma. He developed a technique to noninvasively assess several parameters of aqueous humor dynamics, including outflow facility and uveoscleral outflow, in humans. He, Carol Toris, PhD, and I were some of the first to evaluate latanoprost's mechanism of action in humans. We concluded that the drug acted primarily on uveoscleral outflow.7

For 10 years, Dr. Yablonski led the department of which I am now chair, and he helped to develop it by recruiting many outstanding faculty members. He was a superb mentor who taught me about the intricacies of aqueous humor dynamics, and he was a close friend, whom I sorely miss.

4. What advances in medical therapy for glaucoma do you foresee during the next 10 years?
It will be difficult to find a drug that is more effective and better tolerated than the prostaglandin analogs. In terms of lowering IOP, I expect that the next “advances” will be drugs in the same classes as those that already exist and/or combination products, including formulations coupling beta-blockers and prostaglandin analogs, some of which are already available outside the US. I do not believe that, in the near future, a drug will be approved by the FDA for glaucoma therapy with claims of enhancing ocular blood flow, because it is so difficult to noninvasively assess ocular blood flow relevant to glaucomatous optic neuropathy in humans. It is possible that neuroprotective drugs will be approved for glaucoma therapy. They likely will be drugs already approved for use as neuroprotectants for other diseases. Also, advances may be made in drug delivery to reduce the frequency of drug application to less than once daily. Delivery systems that would enable administration once every several months or longer could be useful in patients who do not adhere to prescribed therapy.

5. What is the current focus of your research?
My colleagues and I are focused on ocular pharmacology, physiology, and therapeutics. We continue to evaluate the mechanism of action of drugs that reduce IOP and to investigate new pharmacological agents. We conduct studies in mice, rabbits, monkeys, and humans. We are interested in how aqueous humor dynamics, including the uveoscleral outflow pathway, are affected by drugs, the circadian rhythm, glaucoma, and age. We investigate the effect of central corneal thickness on IOP as determined by several tonometric devices. In addition, we are studying the mechanisms of optic nerve damage in glaucoma. One of our goals is to develop a drainage device that will make glaucoma surgery safe, effective, predictable, and adjustable as well as quick and easy to perform.

1. Bito LZ. The effects of experimental uveitis on anterior uveal prostaglandin transport and aqueous humor composition. Invest Ophthalmol. 1974;13:959-966.
2. Bito LZ. Active transport of prostaglandins. Prostaglandins. 1974;6:545.
3. Camras CB, Bito LZ, Eakins KE. Reduction of intraocular pressure by prostaglandins applied topically to the eyes of conscious rabbits. Invest Ophthalmol Vis Sci. 1977;16:1125-1134.
4. Camras CB, Bito LZ. Reduction of intraocular pressure in normal and glaucomatous primate (Aotus trivirgatus) eyes by topically applied prostaglandin F2 alpha. Curr Eye Res. 1981;1:205-209.
5. Camras CB, Siebold EC, Lustgarten JS, et al. Maintained reduction of intraocular pressure by prostaglandin F2 alpha-1-isopropyl ester applied in multiple doses in ocular hypertensive and glaucoma patients. Ophthalmology. 1989;96:1329-1336; discussion 1336-1337.
6. Camras CB. Comparison of latanoprost and timolol in patients with ocular hypertension and glaucoma: a six-month masked multicenter trial in the United States. The United States Latanoprost Study Group. Ophthalmology. 1996;103:138-147.
7. Toris CB, Camras CB, Yablonski ME. Effects of PhXA41, a new prostaglandin F2 alpha analog, on aqueous humor dynamics in human eyes. Ophthalmology. 1993;100:1297-1304.